Mycoprotein is a fungal-based ingredient rich in fibre and protein used in meat substitutes called Quorn. Fibre and protein positively regulate glycaemia, lipidaemia and energy intake which are non-communicable diseases’ (NCD) markers. We performed a cross-sectional study to investigate the association of mycoprotein intake with diet quality, nutrient, energy intake and NCD risk within 5507 UK free-living adults from the National Diet and Nutrition Survey from years 2008/2009 to 2016/2017. Dietary approaches to stop hypertension (DASH) and healthy diet index (HDI) were calculated to estimate diet quality. Comparison between mycoprotein consumers (>1 % kcal) and non-consumers, and associations between consumers and nutrient intakes, NCD’s risk markers and diet quality were investigated using a survey-adjusted general linear model adjusted for sex, age, BMI, ethnicity, socio-economic, smoking status, region of residency, total energy, energy density, HDI and non-mycoprotein fibre intake. Mycoprotein consumers (3·44 % of the cohort) had a higher intake of dietary fibre (+22·18 %, P < 0·001), DASH score (+23·33 %) and HDI (+8·89 %) (P < 0·001, both) and lower BMI (−4·77 %, P = 0·00) v. non-consumers. There was an association (P = 0·00) between mycoprotein consumers and diet quality scores (+0·19 and +0·26), high fibre (+3·17 g), total and food energy (+3·09 and +0·22 kcal), but low energy density intakes (−0·08 kcal/g, P = 0·04). Consumers were negatively associated with fasting blood glucose (−0·31 mmol/l, P = 0·00) and glycated HbA1c (−0·15 %, P = 0·01). In conclusion, mycoprotein intake is associated with lower glycaemic markers and energy density intake, and high fibre, energy intake and diet quality scores.

Mycoprotein is a food high in both dietary fibre and non-animal-derived protein. Global mycoprotein consumption is increasing, although its effect on human health has not yet been systematically reviewed. This study aims to systematically review the effects of mycoprotein on glycaemic control and energy intake in humans. A literature search of randomised controlled trials was performed in PubMed, Embase, Web of Science, Google Scholar and hand search. A total of twenty-one studies were identified of which only five studies, totalling 122 participants, met the inclusion criteria. All five studies were acute studies of which one reported outcomes on glycaemia and insulinaemia, two reported on energy intake and two reported on all of these outcomes. Data were extracted, and risk-of-bias assessment was then conducted. The results did not show a clear effect of acute mycoprotein on blood glucose levels, but it showed a decrease in insulin levels. Acute mycoprotein intake also showed to decrease energy intake at an ad libitum meal and post-24 h in healthy lean, overweight and obese humans. In conclusion, the acute ingestion of mycoprotein reduces energy intake and insulinaemia, whereas its impact on glycaemia is currently unclear. However, evidence comes from a very limited number of heterogeneous studies. Further well-controlled studies are needed to elucidate the short- and long-term effects of mycoprotein intake on glycaemic control and energy intake, as well as the mechanisms underpinning these effects.

Dietary mycoprotein decreases energy intake in lean individuals. The effects in overweight individuals are unclear, and the mechanisms remain to be elucidated. This study aimed to investigate the effect of mycoprotein on energy intake, appetite regulation, and the metabolic phenotype in overweight and obese volunteers. In two randomised-controlled trials, fifty-five volunteers (age: 31 (95 % CI 27, 35) years), BMI: 28·0 (95 % CI 27·3, 28·7) kg/m2) consumed a test meal containing low (44 g), medium (88 g) or high (132 g) mycoprotein or isoenergetic chicken meals. Visual analogue scales and blood samples were collected to measure appetite, glucose, insulin, peptide tyrosine-tyrosine (PYY) and glucagon-like peptide-1 (GLP-1). Ad libitum energy intake was assessed after 3 h in part A (n 36). Gastric emptying by the paracetamol method, resting energy expenditure and substrate oxidation were recorded in part B (n 14). Metabonomics was used to compare plasma and urine samples in response to the test meals. Mycoprotein reduced energy intake by 10 % (280 kJ (67 kcal)) compared with chicken at the high content (P=0·009). All mycoprotein meals reduced insulin concentrations compared with chicken (incremental AUClow (IAUClow): −8 %, IAUCmedium: −12 %, IAUChigh: −21 %, P=0·004). There was no significant difference in glucose, PYY, GLP-1, gastric emptying rate and energy expenditure. Following chicken intake, paracetamol-glucuronide was positively associated with fullness. After mycoprotein, creatinine and the deamination product of isoleucine, α-keto-β-methyl-N-valerate, were inversely related to fullness, whereas the ketone body, β-hydroxybutyrate, was positively associated. In conclusion, mycoprotein reduces energy intake and insulin release in overweight volunteers. The mechanism does not involve changes in PYY and GLP-1. The metabonomics analysis may bring new understanding to the appetite regulatory properties of food.

Prospective cohort studies have shown inverse associations between fibre intake and CVD, possibly mediated by blood pressure (BP). However, little is known about the impact of types of fibre on BP. We examined cross-sectional associations with BP of total, insoluble and soluble fibre intakes. Data were used from the INTERnational study on MAcro/micronutrients and blood Pressure (INTERMAP) study, including 2195 men and women aged between 40 and 59 years from the USA. During four visits, eight BP, four 24 h dietary recalls and two 24 h urine samples were collected. Linear regression models adjusted for lifestyle and dietary confounders to estimate BP differences per 2 sd higher intakes of total and individual types of fibre were calculated. After multivariable adjustment, total fibre intake higher by 6·8 g/4184 kJ (6·8 g/1000 kcal) was associated with a 1·69 mmHg lower systolic blood pressure (SBP; 95 % CI −2·97, −0·41) and attenuated to −1·01 mmHg (95 % CI −2·35, 0·34) after adjustment for urinary K. Insoluble fibre intake higher by 4·6 g/4184 kJ (4·6 g/1000 kcal) was associated with a 1·81 mmHg lower SBP (95 % CI −3·65, 0·04), additionally adjusted for soluble fibre and urinary K excretion, whereas soluble fibre was not associated with BP. Raw fruit was the main source of total and insoluble fibre, followed by whole grains and vegetables. In conclusion, higher intakes of fibre, especially insoluble, may contribute to lower BP, independent of nutrients associated with higher intakes of fibre-rich foods.

There is evidence for health benefits from ‘Palaeolithic’ diets; however, there are a few data on the acute effects of rationally designed Palaeolithic-type meals. In the present study, we used Palaeolithic diet principles to construct meals comprising readily available ingredients: fish and a variety of plants, selected to be rich in fibre and phyto-nutrients. We investigated the acute effects of two Palaeolithic-type meals (PAL 1 and PAL 2) and a reference meal based on WHO guidelines (REF), on blood glucose control, gut hormone responses and appetite regulation. Using a randomised cross-over trial design, healthy subjects were given three meals on separate occasions. PAL2 and REF were matched for energy, protein, fat and carbohydrates; PAL1 contained more protein and energy. Plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic peptide (GIP) and peptide YY (PYY) concentrations were measured over a period of 180 min. Satiation was assessed using electronic visual analogue scale (EVAS) scores. GLP-1 and PYY concentrations were significantly increased across 180 min for both PAL1 (P= 0·001 and P< 0·001) and PAL2 (P= 0·011 and P= 0·003) compared with the REF. Concomitant EVAS scores showed increased satiety. By contrast, GIP concentration was significantly suppressed. Positive incremental AUC over 120 min for glucose and insulin did not differ between the meals. Consumption of meals based on Palaeolithic diet principles resulted in significant increases in incretin and anorectic gut hormones and increased perceived satiety. Surprisingly, this was independent of the energy or protein content of the meal and therefore suggests potential benefits for reduced risk of obesity.

In recent years, there has been a renewed interest in the role of dietary fibre in obesity management. Much of this interest stems from animal and human studies which suggest that an increased intake of fermentable fibre can suppress appetite and improve weight management. A growing number of reports have demonstrated that the principal products of colonic fermentation of dietary fibre, SCFA, contribute to energy homeostasis via effects on multiple cellular metabolic pathways and receptor-mediated mechanisms. In particular, over the past decade it has been identified that a widespread receptor system exists for SCFA. These G-protein-coupled receptors, free fatty acid receptor (FFAR) 2 and FFAR3 are expressed in numerous tissue sites, including the gut epithelium and adipose tissue. Investigations using FFAR2- or FFAR3-deficient animal models suggest that SCFA-mediated stimulation of these receptors enhances the release of the anorectic hormones peptide tyrosine tyrosine and glucagon-like peptide-1 from colonic L cells and leptin from adipocytes. In addition, the SCFA acetate has recently been shown to have a direct role in central appetite regulation. Furthermore, the SCFA propionate is a known precursor for hepatic glucose production, which has been reported to suppress feeding behaviour in ruminant studies through the stimulation of hepatic vagal afferents. The present review therefore proposes that an elevated colonic production of SCFA could stimulate numerous hormonal and neural signals at different organ and tissue sites that would cumulatively suppress short-term appetite and energy intake.

While it has been proposed, based on epidemiological studies, that whole grains may be beneficial in weight regulation, possibly due to effects on satiety, there is limited direct interventional evidence confirming this. The present cross-over study aimed to investigate the short-term effects on appetite and food intake of 48 g of whole-grain wheat (daily for 3 weeks) compared with refined grain (control). A total of fourteen healthy normal-weight adults consumed, within their habitual diets, either two whole-grain bread rolls (providing 48 g of whole grains over two rolls) or two control rolls daily for 3 weeks. Changes in food intake were assessed using 7 d diet diaries. Changes in subjective appetite ratings and food intake were also assessed at postprandial study visits. There were no significant differences between interventions in energy intake (assessed by the 7 d diet diaries and at the ad libitum test meal), subjective appetite ratings or anthropometric measurements. However, there was a significant difference between interventions for systolic blood pressure, which decreased during the whole-grain intervention and increased during the control intervention ( − 2 v. 4 mmHg; P = 0·015). The present study found no effect of whole grains on appetite or food intake in healthy individuals; however, 48 g of whole grain consumed daily for 3 weeks did have a beneficial effect on systolic blood pressure. The findings from the present study therefore do not support epidemiological evidence that whole grains are beneficial in weight regulation, although further investigation in other population groups (such as overweight and obese) would be required.

The recently discovered SCFA-activated G-coupled protein receptors FFA receptor 2 and FFA receptor 3 are co-localised in l-cells with the anorexigenic ‘ileal brake’ gut hormone peptide YY, and also in adipocytes, with activation stimulating leptin release. Thus, SCFA such as acetate and propionate show promise as a candidate to increase satiety-enhancing properties of food. We therefore postulate SCFA may have a role in appetite regulation and energy homeostasis. SCFA can be delivered either directly within food, or indirectly via the colon by the provision of fermentable non-digestible carbohydrates. A review of studies investigating the effects of oral SCFA ingestion on appetite suggests that while oral SCFA ingestion is associated with enhanced satiety, this may be explained by product palatability rather than a physiological effect of SCFA. Colon-derived SCFA generated during microfloral fermentation have also been suggested to explain satiety-enhancing properties of non-digestible carbohydrates. However, findings are mixed from investigations into the effects of the prebiotic inulin-type fructans on appetite. Overall, data presented in this review do not support a role for SCFA in appetite regulation.

Resistant starch (RS), a non-viscous dietary fibre, may have postprandial effects on appetite regulation and metabolism, although the exact effects and mechanisms are unknown. An acute randomised, single-blind crossover study, aimed to determine the effects of consumption of 48 g RS on appetite compared to energy and available carbohydrate-matched placebo. Twenty young healthy adult males consumed either 48 g RS or the placebo divided equally between two mixed meals on two separate occasions. Effects on appetite were assessed, using an ad libitum test meal and 24-h diet diaries for energy intake, and using visual analogue scales for subjective measures. Changes to postprandial glucose, insulin and C-peptide were also assessed. There was a significantly lower energy intake following the RS supplement compared to the placebo supplement at both the ad libitum test meal (5241 (sem 313) v. 5606 (sem 345) kJ, P = 0·033) and over the 24 h (12 603 (sem 519) v. 13 949 (sem 755) kJ, P = 0·044). However, there was no associated effect on subjective appetite measures. Postprandial plasma glucose concentrations were not significantly different between supplements, but there was a significantly lower postprandial insulin response following the RS supplement (P = 0·029). The corresponding C-peptide concentrations were not significantly different, although the ratio of C-peptide to insulin was higher following the RS supplement compared to placebo (P = 0·059). These results suggest that consumption of 48 g RS, over a 24-h period, may be useful in the management of the metabolic syndrome and appetite. Further studies are required to determine the exact mechanisms.

Pancreatic polypeptide (PP) is a gut hormone released from the pancreas in response to food ingestion and remains elevated for up to 6 h postprandially. Plasma levels are elevated in patients with pancreatic tumours. An intravenous infusion of PP has been reported to reduce food intake in man, suggesting that PP is a satiety hormone. We investigated whether a lower infusion rate of PP would induce significant alterations in energy intake. The study was randomised and double-blinded. Fourteen lean fasted volunteers (five men and nine women) received 90 min infusions of PP (5 pmol/kg per min) and saline on two separate days. The dose chosen was half that used in a previous human study which reported a decrease in appetite but at supra-physiological levels of PP. One hour after the end of the infusion, a buffet lunch was served and energy intake measured. PP infusion was associated with a significant 11 % reduction in energy intake compared with saline (2440 (se 200) v. 2730 (se 180) kJ; P < 0·05). Preprandial hunger as assessed by a visual analogue score was decreased in the PP-treated group compared to saline. These effects were achieved with plasma levels of PP within the pathophysiological range of pancreatic tumours.

Elevated postprandial glycaemia has been linked to CVD in a number of different epidemiological studies involving predominantly non-diabetic volunteers. The MiniMed continuous glucose monitor, which measures blood glucose every 5 min, over a 24 h period, was used to investigate changes in blood glucose readings before and after instigating a diet with low glycaemic index (GI) for 1 week in free-living healthy individuals. Nine healthy people (age 27 (sem 1·3) years, BMI 23·7 (sem 0·7) kg/m2, one male, eight females) completed the study. A reduction in GI (59·7 (sem 2) v. 52·1 (sem 2), P<0·01) occurred in all nine subjects while energy and other macronutrients remained constant. A significant reduction was also observed in fasting glucose at 06·00 hours (5·4 (sem 0·2) v. 4·4 (sem 0·3) mmol/l, P<0·001), mean glucose (5·6 (sem 0·2) v. 5·1 (sem 0·2) mmol/l, P=0·004), area under the 24 h glucose curve (8102 (sem 243) v. 750 (sem 235) mmol/l per min, P=0·004) and area under the overnight, 8 h glucose curve (2677 (sem 92) v. 2223 (sem 121) mmol/l per min, P=0·01). The present study provides important data on how a simple adjustment to the diet can improve glucose profiles that, if sustained in the long term, would be predicted from epidemiological studies to have a favourable influence on CVD.

Subjects with insulin resistance have been shown to have higher storage levels of intramyocellular lipid (IMCL) than their insulin-sensitive counterparts. It has been proposed that elevated IMCL stores may be the main cause of insulin resistance. The aim of the present study was to ascertain whether there is a causal relationship between IMCL storage and insulin resistance. IMCL storage was assessed using magnetic resonance spectroscopy and insulin sensitivity was assessed by performing an oral glucose tolerance test. A 4-week intervention of reduction of dietary glycaemic index was used to manipulate insulin sensitivity in a cohort of healthy volunteers; the effects of this intervention on IMCL were measured after 4 weeks of intervention. Significant improvements in the insulin sensitivity index occurred following the dietary intervention (baseline 7·8 (sem 1·11) v. post-intervention 9·7 (sem 1·11), P=0·02). However, there were no changes in IMCL storage levels, suggesting that insulin sensitivity can be manipulated independently of IMCL. This suggests that in healthy volunteers, insulin sensitivity is independent of IMCL storage and the high storage levels that have been found in insulin-resistant subjects may occur as a consequence rather than a cause of insulin resistance.

Postprandial concentrations of glucose, insulin and triacylglycerols (TG) correlate to risk for CHD. Carbohydrates affect many metabolites that could have a potential effect on cardiovascular risk factors. The objective of the present study was to examine, using a randomised prospective study, the acute (day 1) and ad libitum medium-term (day 24) effects of four diets: a high-fat diet (HIGH-FAT; 50 % fat, >34 % monounsaturated fatty acids); a low-glycaemic index (GI) diet (LOW-GI; high-carbohydrate, low-GI); a high-sucrose diet (SUCROSE; high carbohydrate increase of 90 g sucrose/d); a high-GI diet (HIGH-GI; high-carbohydrate, high-GI). Daytime profiles (8 h) (breakfast, lunch and tea) of lipid and carbohydrate metabolism were completed during day 1 and day 24. Seventeen middle-aged men with one or more cardiac risk factors completed the study. There was no change from day 1 or between diets in fasting glucose, lipids or homeostatic assessment model (HOMA) on day 24. The HIGH-FAT compared with the three high-carbohydrate diets was associated with lower postprandial insulin and glucose but higher postprandial TG and non-esterified fatty acids (NEFA). There was a significant increase in the 6 h (15.00 hours) TG concentration (day 1, 2·6 (SEM 0·3) MMOL/L v. DAY 24, 3·3 (sem 0·3) mmol/l; P<0·01) on the SUCROSE diet. Postprandial HOMA (i.e. incremental area under the curve (IAUC) glucose (mmol/l per min)×IAUC insulin/22·5 (mU/l per min)) median changes from day 1 to day 24 were −61, −43, −20 and +31 % for the HIGH-FAT, LOW-GI, SUCROSE and HIGH-GI diets respectively. The HIGH-GI percentage change was significantly different from the other three diets (P<0·001). Despite being advised to maintain an identical energy intake there was a significant weight change (−0·27 (sem 0·3) kg; P<0·02) on the LOW-GI diet compared with the SUCROSE diet (+0·84 (sem 0·3) kg). In conclusion the HIGH-FAT diet had a beneficial effect on postprandial glucose and insulin over time but it was associated with higher postprandial concentrations of TG and NEFA. Conversely the HIGH-GI diet appeared to increase postprandial insulin resistance over the study period.